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provide evidence that both CREBBP and EP300 (zeige EP300 Proteine) are bona fide tumor suppressors that control MHCII expression and promote tumor immune control; mutational inactivation of CREBBP, but not of EP300 (zeige EP300 Proteine), has additional cell-intrinsic engraftment and growth-promoting effects
BRD, PHD (zeige PDC Proteine), and ZZ domains interact with SUMO-1 (zeige SUMO1 Proteine) and Ubc9 (zeige UBE2I Proteine), and function as an intramolecular E3 ligase for SUMOylation of the cell cycle regulatory domain 1; the BRD is essential for histone H3 (zeige HIST3H3 Proteine) acetylation
CREBBP Mutation is associated with Rubinstein-Taybi Syndrome and Medulloblastoma.
The recruitment of COASY (zeige COASY Proteine) inhibits CBP-mediated TPX2 (zeige TPX2 Proteine) acetylation, promoting TPX2 (zeige TPX2 Proteine) degradation for mitotic exit.
GATA3 (zeige GATA3 Proteine) interacts with and is acetylated by the acetyltransferase CBP. The major acetylated site of GATA3 (zeige GATA3 Proteine) in lung adenocarcinoma cells is lysine 119.
The mechanism of CBP-CREB (zeige CREB1 Proteine) association via their pKID/KIX domains studied by molecular dynamics free energy simulations has been reported.
Our study demonstrated the association of low CREBBP expression with adverse clinical and biological features, poor prednisone response, high MRD levels and inferior outcomes in paediatric Chinese patients with ALL who were treated with the BCH (zeige CHN2 Proteine)- 2003 and CCLG- 2008 pro- tocols.
Knockdown of CREB (zeige CREB1 Proteine) suppressed the expression of matrix metallopeptidase (zeige ECEL1 Proteine) (MMP)2 (zeige MMP2 Proteine)/9.
Ectopic expression of EP300 (zeige EP300 Proteine)-ZNF384 (zeige ZNF384 Proteine) and CREBBP-ZNF384 (zeige ZNF384 Proteine) fusion altered differentiation of mouse hematopoietic stem and progenitor cells and also potentiated oncogenic transformation in vitro.our results indicate that gene fusion is a common class of genomic abnormalities in childhood ALL and that recurrent translocations involving EP300 (zeige EP300 Proteine) and CREBBP may cause epigenetic deregulation with potential for therapeutic targeting.
The CREBBP acetyltransferase is a haploinsufficient tumor suppressor in B-cell lymphoma.
Data (including data from studies in knockout and transgenic mice) suggest that Ep300 (zeige EP300 Proteine) and Crebbp are limiting cofactors for pancreatic islet development (including gene expression regulation and cell proliferation), and hence for postnatal glucose homeostasis, with some functional redundancy. (Ep300 (zeige EP300 Proteine) = E1A binding protein p300 (zeige EP300 Proteine); Crebbp = CREB binding protein)
Enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation
the aPKC-CBP pathway is a homeostatic compensatory mechanism that modulates hippocampal neurogenesis and memory in an age-dependent manner in response to reduced CREB (zeige CREB1 Proteine) activity.
Earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies.
High CBP-P300 expression is associated with lymphoma.
This study provides evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 (zeige BCL2 Proteine) overexpression to promote B-cell lymphoma.
Data (including data from studies of hydrogen-deuterium exchange coupled to mass spectrometry in presence of denaturants) suggest that, for peptide fragments of human ACTR (zeige NCOA3 Proteine) and mouse Crebbp representing disordered interaction domains, exchange rates are changed dramatically by high concentrations of denaturants guanidinium chloride or urea. (ACTR (zeige NCOA3 Proteine) = activator of thyroid and retinoid receptor; Crebbp = CREB binding protein)
Crebbp+/- common myeloid progenitors and granulocyte/macrophage progenitors could trigger skewed myelopoiesis, myelodysplasia and late-onset acute myeloid leukemia (zeige BCL11A Proteine).
This gene is ubiquitously expressed and is involved in the transcriptional coactivation of many different transcription factors. First isolated as a nuclear protein that binds to cAMP-response element binding protein (CREB), this gene is now known to play critical roles in embryonic development, growth control, and homeostasis by coupling chromatin remodeling to transcription factor recognition. The protein encoded by this gene has intrinsic histone acetyltransferase activity and also acts as a scaffold to stabilize additional protein interactions with the transcription complex. This protein acetylates both histone and non-histone proteins. This protein shares regions of very high sequence similarity with protein p300 in its bromodomain, cysteine-histidine-rich regions, and histone acetyltransferase domain. Mutations in this gene cause Rubinstein-Taybi syndrome (RTS). Chromosomal translocations involving this gene have been associated with acute myeloid leukemia. Alternative splicing results in multiple transcript variants encoding different isoforms.
, CREB binding protein (Rubinstein-Taybi syndrome)